These observations suggest that EVs from virus-activated platelets play as endogenous danger signals to trigger NETs and inflammatory reactions via CLEC5A and TLR2, and blockade of CLEC5A and TLR2 may become a promising strategy to attenuate SARS-CoV-2-induced thrombus and coagulopathy in COVID-19 patients in the future. The gene discussed is TLR2; the disease is COVID-19.